urge to breathe ("break point"), and an involuntary gasp results (60,76,86). During the period of breath-holding, the victim is unable to cry for help (73,88). The mean duration of voluntary breath-holding is about 1.5 min in trained individuals compared with about 1 min in the average person (89). The duration of breath-holding is decreased when the victim is immersed in cold water (see Subheading 4.5. and ref. 60).
Following the involuntary gasp, variable laryngospasm occurs when water contacts the glottis (47,58,76,86). More water can also be swallowed at this stage (47). When water is inhaled, a parasympathetic (vagal) reflex causes peripheral airway constriction and increased resistance, resulting in reduced lung compliance (see Subheading 4.3. and refs. 58, 60, 76, 90, and 91). Intrapulmonary shunts are created in fresh and salt water submersion by different mechanisms. Inhaled water, contacting the alveolar membrane, affects surfactant (76,78). Experimental studies of dogs showed hyperosmolar, i.e., osmolarity greater than human plasma (e.g., sea water), and iso-osmolar saline solutions dilute or wash out surfactant (58,60,76,81). Fresh water, chlorinated or nonchlorinated, damages the alveolar membrane and decreases surfactant. Impurities in water (dirt, sewage, detergents) are also injurious (see Subheading 4.4.). Alveolar collapse (atelectasis) leads to intrapulmonary shunting and ventilation-perfusion mismatch (58,76,78,82,83,85,92). Disturbed pulmonary reflex responses are of prime importance in the clinical setting (73,83). In saltwater drowning, intrapulmonary shunting results when fluid is drawn from the circulation into the alveolar spaces (47,78,83,86,92). Pulmonary edema occurs not only in saltwater drowning but also in freshwater submersion. Although fresh water is absorbed rapidly into the circulation, hypoxia depresses cardiac function. This and altered alveolar capillary permeability result in an alveolar transduate (84,93,94). The evolution of hypoxia is multifactorial, arising from reduced ventilation owing to laryngospasm, large airway obstruction by froth (edema fluid mixed with water and air), mucus and foreign material, airway constriction, atelectasis, and intra-alveolar edema (60,74,78,90). No difference in survival has been observed in fresh and saltwater drownings; however, rescue services may be better on coastal shores, compared with inland bodies of water, meaning expeditious resuscitation and survival (46,73,88).
Although pulmonary edema is common, changes in blood volume and electrolyte disturbances, as seen in animal experiments (hemoconcentration in saltwater cases; hemolysis, hemodilution, hyponatremia, and hyperkalemia in freshwater aspiration), are usually insignificant in the clinical setting (47,50,58,60,78,80-82,85,88,92,94-97). Generally, the cardiovascular and pulmonary changes associated with the aspiration of water are not dependent on its tonicity (98,99). Changes in intravascular volume in fresh and saltwater drowning are transient in the clinical setting, owing to the body's compensatory mechanisms (47). Electrolyte imbalance can arise from aspiration of large volumes of water. In animal experiments, large volumes (44 mL/kg or 20 mL/lb) of fresh water does cause electrolyte disturbances and hemolysis, but this quantity is unlikely to be aspirated in humans (2,73,100). Research has shown that inhalation of 22 mL/kg (or 10 mL/lb) is associated with normal electrolyte levels (74,78). This was observed in dog experiments, which showed that electrolyte changes were transient and ventricular fibrillation from hyperkalemia did not occur (82,95). One study of drowning victims in fresh and salt water showed that 15% of individuals had inhaled more than 22 mL/kg (10 mL/lb) of water, causing significant changes in chloride levels in the left ventricle (80). Ventricular fibrillation caused by electrolyte disturbance is uncommon in the clinical setting (85,88,95). In animal research, aspiration of 2.2 mL/kg (1mL/lb) of water causes hypoxia within a few minutes (58,73,76,82,85,92-94). Aspiration of small amounts of water is applicable to near-drowning. There are clinical reports that describe abnormalities resulting from volume and electrolyte changes. For example, significant hemolysis can trigger disseminated intravascular coagulation (DIC [101 ]). Changes in electrolytes owing to saltwater aspiration are a function of the volume and concentration of the medium (79). Very salty water (e.g., submersion in the Dead Sea) can lead to serum electrolyte changes, but pulmonary pathophysiological complications are still paramount in the clinical management (102).
After the first submerged breath and aspiration of water, secondary apnea follows within seconds (60). There is involuntary gasping under water for several minutes, culminating in respiratory arrest (88). Increasing hypoxia leads to arrhythmias, cardiac arrest, and eventual brain death, if resuscitation is not timely. Unconsciousness from cerebral hypoxia happens within 3 min of involuntary submersion (103). The duration of hypoxia leading to irreversible cerebral damage is age-dependent. Witnessed accounts of immersion time in fatal drownings are estimates at best, and vary depending on age and water temperature (e.g., 3-10 min, if water temperature above 15-20°C [59-68°F]; survival of some children, and even return of normal neurological function, following 5-40 min of immersion in water at 0-15°C [32-59°F]; see Subheading 4.5. and refs. 60, 76, and 103). A study of bathtub immersions showed survival of children who were submerged from 3 to 5 min (median 4 min), and deaths when the immersion time ranged from 3 to 20 min (median 5 min ).
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